GI3 Flashcards
best practices for paracentesis
- explain proceedure
- vitals w weight
- void prior to proceedure
- elevate head of bed
- monitor vital
- measure drainage accurately record, describe, lable and send to lab
- dress site, bedrest per protocol
- weigh pt and record difference
cirrhosis meds
INDERAL- beta blocker to help prevent bleeding ( reduces heart rate and hepatic venous pressure gradient)
Vasopressin and Sandostatin will reduce blood flow through vasoconstriction to decrease portal pressure
Sandostatin suppresses secretion of gastrin, serotonin and intestinal peptides which helps decrease GI blood flow
ascites causes
Increased hydrostatic pressure from portal hypertension
More plasma proteins are in the peritoneal fluid rather the vascular system. The liver does not produce albumin as well. This results in low protein in the circulatory system
The patient will have hypovolemia as well as third spacing in the peritoneal cavity along with edema
Massive ascites put pressure on the kidney which triggers the renin-angioretensin system. This causes sodium and water retentions which increases swelling
nutrition therapy for a pt w liver disease
low sodium, vitamins, high carb mederate fat, low protein
lab value abnormalities that increase risk of bleeding w end stage liver disease
elevated ast, alt, bili, PT, INR
decreased total protein, albumin
clay colored stool
inability of failing liver to excrete bilirubin
jaundice causes
intrahepatic obstruction from edema to the bile channels, elevated serum total bilirubin
hepatitis vaccines
A and B
Hep A risk factors
Spread most often by fecal oral route Flu like infection that may go unrecognized Oral anal or contaminated food or water Shellfish or food handlers Incubation period 15-20 days
Hep B risk factors
Blood and fluid transmission
Sex, needles, transfusions (now screened after 1992), Hemodialysis
Immunosuppressed more likely to develop
Incubation period 25-180 days
Many people with Hep B do not exhibit sx. If they do they might have jaundice, fever, joint pain, anorexia, N/V, RUQ pain, dark urine with light stool
Most adults who get Hepatitis B are able to clear it from their bodies and develop immunity
Small amount people do not develop immunity but become carriers
Hep C risk factors
Spread blood to blood
Blood or organ transplants received before 1992
Illicit drug use (highest incidence)
Unsanitary tattoos
Sharing intranasal cocaine equipment
Do not share razors, toothbrushes or pierced earrings
Average incubation period 7 weeks
May be asymptomatic for months or years after initial exposure
Acute infection not common
Most people DO NOT clear the virus and chronic infection develops
common signs of elevated ammonia levels (hepatic encephalopathy) stage 1
subtle, may not be recognized immediately
- personality, behavior, emotional, thinking, concentration
- fatigue, slurred/slowed speech, sleep disturbances
common signs of elevated ammonia levels (hepatic encephalopathy) stage 2
continuing mental changes
- confusion, disorientation to time, place, person
- asterixis (hand flapping)
common signs of elevated ammonia levels (hepatic encephalopathy) stage 3
progressive deteriorentation
- marked mental confusion
- stuporous, drowsy but arousable
- abnormal ECG, muscle twitching, hyperreflexia
- asterixis
common signs of elevated ammonia levels (hepatic encephalopathy) stage 4
unresponsive, obtunded, no asterixis
- positive babinski
- muscle rigidity
- fetor hepaticus-musty sweet liver breath
- seizures/death
lactulose
promotes excretion of ammonia in stool. Draws fluid into colon and reduces the absorption of ammonia into colon. Hypokalemia and dehydration may occur with all of the loose stools
propranolol
lower portal pressure and inhibit renin secretion with ascites
spironolactone
diuretic for ascites, conserves potassium
hepatic encephalopathy diet changes
moderate protein and fat and simple carbs
cholecystits risk facotrs
fat, fair, forty, female, fertile
cholecystits diagnostic tests
ultrasound, abdominal xray, HIDA scan, ERCP, MRCP
diet changes after chole
avoid high fat foods
pathophysiology of acute pancreatitis
Stage 1 lipolysis
Hallmark of pancreatitis is Lipolysis causing fatty acids to be released which combine with calcium. The calcium drops quickly. The parathyroid glands can’t keep up to raise the calcium so hypocalcemia develops.
pathophysiology of acute pancreatitis
Stage 2 proteolysis
Proteolysis is the breakdown of proteins. May lead to thrombosis and gangrene
pathophysiology of acute pancreatitis
Stage 3 necrosis of blood vessels
Elastase causes blood vessels and ducts to breakdown
Kallikrein ( another enzyme) triggers release of other chemicals that cause vasodilation and increase vascular permeability
pathophysiology of acute pancreatitis
Stage 4 inflammatory stage
Inflammatory stage – WBC gather around area of hemorrhage and necrosis. If infection severe calcification and fibrosis occur. Abscess may be walled off and become a pseudocyst
complications of acute pancreatitis
jaundice, hemorrhage, acute kidney failure, paralytic ileus
- hypovolemic shock, pleural effusion, ARDS, atelectasis
- pneumonia, MSOF, DIC, DM2
etiology of acute pancreatitis
biliary tract disease, trauma (surgical, diagnostic tests, external)
-tumors, cysts, metabolic disorders, ulcers, familial pancreatitis, cystic fibrosis, drug toxicities, alcoholism, smoking
chronic pancreatitis interventions
pain management
PERT- pancreatic enzymen replacement therapy prevents malnutrition, malabsorption, and excessive weight loss-don’t give w H2 blockers, don’t mix w protein, monitor uric acid levels
-need 4000-6000 calories a day
-high carb, high protein, low fat
pancreatic abcess
fatal if untreated, high recurrance rate, high fever
pancreatic pseudocyst
no epithelial lining, form on or around pancreas, palpated, epigastric pain radiating to back, may spontaneously resolve or rupture
pancreatic cancer complications
venous thromboembolism, late detection, highly metastatic
post op care w open radiac pancreaticoduodenectomy-whipple
maintain fluid and electrolyte balance, significant blood loss (hypovolemia), decreased BP w increased HR, decrease urine output, pitting edema, monitor glucose, NPO w NG
